17 research outputs found
rRNA METHYLTRANSFERASES AND THEIR ROLE IN RESISTANCE TO ANTIBIOTICS rRNK METILTRANSFERAZE I NJIHOVA ULOGA U REZISTENCIJI NA ANTIBIOTIKE
MTaze metiluju nukleinske kiseline (DNK, RNK) i proteine, moduli{u}i tako njihovu aktivnost, funkciju i strukturnu organizaciju. Metilacija G1405 ili A1408 baza u 16S rRNK mikroorganizama koji proizvode aminoglikozide obezbe |u -je rezistenciju na sopstvene toksi~ne pro izvode. Ovaj mehanizam rezistencije je donedavno bio opi san samo kod proizvo|a~a antibiotika. Od 2003. godine i kod patogenih bakterija bele`i se neprestan porast rezi sten cije na aminoglikozide putem ovog mehanizma, {to predstavlja veliku pretnju efikasnoj upotrebi aminoglikozida u klini~koj praksi. Jedno od mogu}ih re{enja problema le`i u razvoju novih jedinjenja koja bi efikasno delovala na nova mesta u okviru ribozoma. Drugi pristup re{avanju ovog problema uklju~uje razvoj inhibitora MTaza odgovornih za rezisten ciju, sa idejom da se onemogu}i modifikacija bakte rijske rRNK i na taj na~in vrati terapeutska efikasnost postoje}im aminogliko zidima. Fundamentalna istra`ivanja vezana za proteinsku ekspresiju, potpuno razumevanje mehanizma rezistencije kao i razre{enje tercijarne strukture proteina su neophodan preduslov za primenu inhibitora 16S rRNK MTaza u medicini
Der Grabherr und sein Frau : zur Ikonographie der Status- und Machtverhältnisse in den Privatgräbern des Alten Reiches
chromatography of phenolic compounds
Factorial design in isocratic high-performance liqui
Original scientific paper Expression and purification of the Sgm protein from E. coli
Abstract: Thesgm gene from Micromonospora zionensis, the producer of the aminoglycoside antibiotic G-52, encodes for Sgm methylase which modifies the target site on 16S rRNAand thus protects the producer against its own toxic product. The sgm gene was modified by polymerase chain reaction (PCR) and cloned in the QIAexpress pQE-30 vector in order to make a construct that places the (His) 6 tag at the N-terminus of the protein. The resulting expression construct was transformed in the E. coli strain NM522 and the functional activity of the Sgm-His fusion protein was confirmed in vivo. Purification of the (His) 6-tagged Sgm protein by Ni-NTA affinity chromatography was performed under native conditions and the protein was detected on a sodium dodecyl sulfate polyacrylamide gel. Sgm methylase was purified to homogeneity> 95 %. Polyclonal antibodies raised to purified (His) 6-tagged Sgm protein were used to identify this protein by Western blot analysis
Original paper EFFECTS OF VARIOUS NITRIC OXIDE SYNTHASE INHIBITORS ON QUINOLINIC ACID-INDUCED NEURONAL INJURY IN RATS
Summary: The aetiology of neuronal death in neurodegenerative diseases, including Huntington’s disease, is still unknown. There could be a complex interplay among altered energy metabolism, excitotoxicity and oxidative stress. Our aim was to examine the effects of intrastriatal injection of a selective inhibitor of neuronal nitric oxide synthase, 7-nitroindazole, and a non-specific potent nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester, in order to study the possible involvement of glutathione, an important antioxidant, in quinolinic acid-induced striatal toxicity in the rat. Unilateral administration of quinolinic acid to rat striatum in a single dose of 150 nmol/L was used as a model of Huntington’s disease. The other group of animals were pretreated with 7-nitroindazole and Nw-nitro-L-arginine methyl ester, respectively. Control groups were treated with saline solution and olive oil, respectively. Content of total glutathione, was increased in the ipsi- and contralateral striatum, forebrain cortex, basal forebrain and hippocampus in the groups treated with nitric oxid synthase inhibitors and quinolinic acid compared to the quinolinic acid-treated animals. These results support the hypothesis that oxygen free radicals contribute to excitotoxic neuronal injury, and also that nitric oxide synthase inhibitors could be potential neuroprotective agents in Huntington’s disease. Key words: Huntington’s disease; quinolinic acid; Nw-nitro-L-arginine methyl ester; 7-nitroindazole; glutathion
Functionalization of cellulose fibres with DOPO-polysilsesquioxane flame retardant nanocoating
The preparation of 9,10-dihydro-9-oxa-10-phosphaphenanthrene-10-oxide-functionalised polysilsesquioxane (Si-DOPO)-coating was described and its flame retardant efficiency for cotton fabric was thoroughly investigated. The 9,10-dihydro-9-oxa-10-phosphaphenanthrene-10-oxide\u2013vinyltrimethoxysilane (DOPO\u2013VTS) was synthesized and applied to cotton fabrics at different concentrations using a sol\u2013gel process. The structure of the synthesized DOPO\u2013VTS was characterized using Fourier-transform infrared spectroscopy and nuclear magnetic resonance spectroscopy. The characteristics of the Si-DOPO coatings formed on the cotton fibres were investigated using X-ray photoelectron spectroscopy, time-of-flight-secondary ion mass spectrometry and scanning electron microscopy. The flame retardant properties of the Si-DOPO-coated cotton samples were evaluated by thermogravimetric analyses, vertical flame spread tests and cone calorimetry analyses. The Si-DOPO coating increased the thermo-oxidative stability of the cotton fibres by increasing the stability of the protective char and inhibited cellulose fibres degradation. The Si-DOPO coating did not decrease the time of flaming combustion but did completely stop the vigorous combustion of the fibres. The results also suggest that the flame retardation by the Si-DOPO coating is due to the quenching of active radicals from the decomposing cellulose and the cellulose phosphorylation by the DOPO component as well as the silicon oxide formation by the silsesquioxane component on the fibre surface. These findings indicate that the flame retardant efficiency of the Si-DOPO coating can be ascribed to the combined activity of phosphorus acting in both gas and condensed phases and silicon acting in the condensed phase
Exploring In-hospital Death from Myocardial Infarction in Eastern Europe; From the International Registry of Acute Coronary Syndromes in Transitional Countries (ISACS-TC); on the behalf of the Working Group on Coronary Pathophysiology & Microcirculation of the European Society of Cardiology
Introduction: The aim of the current study was to investigate the outcomes of coronary reperfusion therapies and ST-segment elevation myocardial infarction (STEMI) in patients of eastern countries with economies in transition. Methods and Results: We received STEMI registry data from 4 countries: Bosnia and Herzegovina, Hungary, Russian Federation, and Serbia. The overall population consisted of 23,486 consecutive patients admitted to hospitals from January 1st to December 31st 2009. Registry data and statistics from the Organization for Economic Cooperation and Development (OECD) countries for the same period were used for comparison (2009-2010). In-hospital mortality was between 4% and 5% in the Western countries. In comparison mortality data was significantly larger in Serbia (10.8%) and Bosnia and Herzegovina (11.2%), intermediate in Russian Federation (7.2%) and similar in Hungary (5.0%). The rates of primary percutaneous coronary intervention (primary PCI) were very low in Bosnia and Herzegovina (18.3%), low in Russian Federation (20.6%) and Serbia (22%), and high in Hungary (70%). Major risk factors for death appear to be lack of reperfusion therapy, longer time delay from symptoms onset to hospital presentation as well as the higher percentage of patients with clinical presentation in Killip class III/IV. Conclusion: In-hospital STEMI case-fatality rates ranges widely in the former Eastern Bloc countries. Beyond the quality of care provided in hospitals, differences in time delay from symptoms onset to hospital admission may strongly influence STEMI patients' outcome